+publisher:"Penn State University" +contributor:("Henry Joseph Donahue, Committee Chair/Co-Chair")

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Penn State University

1. Lloyd, Shane. The Role of Connexin43 Gap Junction Protein in the Musculoskeletal Changes Induced by Mechanical Unloading.

Degree: 2013, Penn State University

URL: https://submit-etda.libraries.psu.edu/catalog/18342

► Connexin43 (Cx43) is the predominant gap junction protein in bone. In the present study we examined the role of Cx43 in the skeletal response to… (more)

▼ Connexin43 (Cx43) is the predominant gap junction protein in bone. In the present study we examined the role of Cx43 in the skeletal response to mechanical unloading (i.e., lack of weight bearing). Mechanical unloading induces significant bone loss and muscle atrophy. A better understanding of the mechanisms underlying these deleterious effects is required in order to identify novel targets for therapeutic countermeasures. First, we collected tissue from mice following 0, 7, 14, and 21 days of hindlimb suspension (HLS) or normal loading. We found that muscle atrophy (due to decreased protein synthesis and increased protein degradation) precedes bone loss during mechanical unloading. Reduced mechanical force due to muscle atrophy may compound bone loss associated with a lack of weight bearing. Furthermore, age-related trabecular bone loss in mice, similar to that which occurs in mature astronauts, is superimposed on unloading. Preservation of muscle mass, cortical bone structure, and overall bone strength with age in normally loaded control mice suggests that muscle has a greater effect on cortical versus trabecular bone. Next, we sought to determine the role of Cx43 in unloading-induced bone loss by subjecting mice with a bone-specific deletion of Cx43 (cKO) to HLS. Following three weeks of HLS, wild-type (WT) mice experienced substantial bone loss; however, these deleterious effects were attenuated in cKO mice. Unloading also suppressed bone formation in WT mice, while there was no change from baseline for cKO-Suspended. mRNA levels of the gene encoding sclerostin, an osteocyte-derived inhibitor of bone formation, were greater in WT-Suspended, whereas cKO-Suspended was unchanged. The proportion of sclerostin-positive osteocytes was significantly lower in cKO-Control versus WT-Control, a difference accounted for by the presence of numerous empty lacunae and apoptotic osteocytes. There was no change in trabecular osteocyte viability. Osteoclast indices were lower in Suspended cKO versus WT-Suspended. Osteocyte apoptosis induced by Cx43 deficiency appears to preserve bone structure by preventing both suppression of bone formation and increased bone resorption during mechanical unloading. Attenuated trabecular bone loss, despite an apparent lack of affect on osteocyte viability in this compartment, suggests that an additional mechanism, independent of osteocyte apoptosis, may also be important. Advisors/Committee Members: Henry Joseph Donahue, Dissertation Advisor/Co-Advisor, Chair%22%29&pagesize-30">Henry Joseph Donahue, Committee Chair/Co-Chair, Charles H Lang, Committee Member, Neil Sharkey, Committee Member, James Robert Connor, Committee Member, Alicia Ellen Bateman, Special Member.

Subjects/Keywords: connexin43; unloading; bone loss; sclerostin; osteocyte; apoptosis; RANKL; muscle; spaceflight; atrophy; osteopenia

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APA (6^th Edition):

Lloyd, S. (2013). The Role of Connexin43 Gap Junction Protein in the Musculoskeletal Changes Induced by Mechanical Unloading. (Thesis). Penn State University. Retrieved from https://submit-etda.libraries.psu.edu/catalog/18342

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Lloyd, Shane. “The Role of Connexin43 Gap Junction Protein in the Musculoskeletal Changes Induced by Mechanical Unloading.” 2013. Thesis, Penn State University. Accessed March 06, 2021. https://submit-etda.libraries.psu.edu/catalog/18342.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Lloyd, Shane. “The Role of Connexin43 Gap Junction Protein in the Musculoskeletal Changes Induced by Mechanical Unloading.” 2013. Web. 06 Mar 2021.

Vancouver:

Lloyd S. The Role of Connexin43 Gap Junction Protein in the Musculoskeletal Changes Induced by Mechanical Unloading. [Internet] [Thesis]. Penn State University; 2013. [cited 2021 Mar 06]. Available from: https://submit-etda.libraries.psu.edu/catalog/18342.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Lloyd S. The Role of Connexin43 Gap Junction Protein in the Musculoskeletal Changes Induced by Mechanical Unloading. [Thesis]. Penn State University; 2013. Available from: https://submit-etda.libraries.psu.edu/catalog/18342

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Penn State University

2. Chin-quee, Karis P. Breast cancer cell secretions promote a pre-metastatic niche in bone; an in vitro look .

Degree: 2013, Penn State University

URL: https://submit-etda.libraries.psu.edu/catalog/17496

► ABSTRACT Successful metastasis requires some degree of hospitality from the host organ that is metastasized. In recent years, evidence has been mounting that the primary… (more)

▼ ABSTRACT Successful metastasis requires some degree of hospitality from the host organ that is metastasized. In recent years, evidence has been mounting that the primary tumor contributes to adapting this remote organ to increase this hospitality. Interestingly, many in vitro experiments have shown that conditioned media from cancer cells produce physical changes which theoretically could facilitate invasion. These include perturbations in extracellular matrix and of cell to cell adhesions. The conditioned media in these in vitro experiments could be interpreted to be a proxy for either paracrine or endocrine effects, however, when these observations are coupled with evidence from in vivo experiments, it seems possible that primary tumors have remote effects on un-metastasized organs that can elicit changes in them which are pro-metastatic. We have performed a series of experiments designed to characterize and describe changes in osteoblasts (hFOB) which occur as a result of exposure to conditioned medium from breast cancer cells (MDA-MET). Functional experiments aimed at investigating whether these changes are pro-metastatic were included as a means of this characterization. Thus cell to cell adhesions, as well as the ability of the osteoblastic environment to attract MDA-MET cells were both assessed. Further, we investigated mechanistically the bases behind the observations from the functional experiments. Methods Confluent hFOB cells were treated with conditioned media from either MDA-MET, MDA-MB-231 HTERT-HME1 or hFOB cells 24 hrs. This treatment conditioned medium was removed, the cells washed and serum-free medium added to the hFOB cells. hFOB-conditioned medium was collected after 18hrs. This medium was then used in in vitro migration assays measuring number of MDA-MET migratory cells by labeling the cells with DNA-binding dye Cyquant; in establishing presence of collagen by western blot; in collagenase assays and in a cytokine array where antibodies to 74 cytokines were embedded on a membrane. The presence of Type 1 collagen receptors was shown by immunocytochemistry. The data were analyzed using one way ANOVA and the Student’s T test. Results We found that conditioned medium from hFOB cells that had been treated with MDA-MET-conditioned medium attracted more MDA-MET cells than hFOB cells pre-exposed to its own medium only. We hypothesized that Type 1 collagen fragments of specific length were the chemoattractants responsible for our observed effect. This was evidenced by an increase in collagenase in the conditioned medium of hFOB cells which had been exposed to MDA-MET-conditioned medium. The definitiveness of this evidence was aided by the inherent fidelity of the collagenase enzymes and its Type 1 collagen substrate and the distinctiveness of the product of this enzyme substrate interaction. We also showed that bacterial collagenase, which creates short collagen fragments of non-specific length removed the ability of hFOB -conditioned medium to attract MDA-MET cells. In addition, we showed that at… Advisors/Committee Members: Henry Joseph Donahue, Dissertation Advisor/Co-Advisor, Chair%22%29&pagesize-30">Henry Joseph Donahue, Committee Chair/Co-Chair, Andrea Manni, Committee Member, Andrea Marie Mastro, Committee Member, David Feith, Committee Member, Lisa M Shantz, Committee Member, Ralph Lauren Keil, Committee Member.

Subjects/Keywords: breast cancer metastasis; pre-metastatic niche; bone; collagen fragments; collagenase

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APA (6^th Edition):

Chin-quee, K. P. (2013). Breast cancer cell secretions promote a pre-metastatic niche in bone; an in vitro look . (Thesis). Penn State University. Retrieved from https://submit-etda.libraries.psu.edu/catalog/17496

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Chin-quee, Karis P. “Breast cancer cell secretions promote a pre-metastatic niche in bone; an in vitro look .” 2013. Thesis, Penn State University. Accessed March 06, 2021. https://submit-etda.libraries.psu.edu/catalog/17496.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Chin-quee, Karis P. “Breast cancer cell secretions promote a pre-metastatic niche in bone; an in vitro look .” 2013. Web. 06 Mar 2021.

Vancouver:

Chin-quee KP. Breast cancer cell secretions promote a pre-metastatic niche in bone; an in vitro look . [Internet] [Thesis]. Penn State University; 2013. [cited 2021 Mar 06]. Available from: https://submit-etda.libraries.psu.edu/catalog/17496.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Chin-quee KP. Breast cancer cell secretions promote a pre-metastatic niche in bone; an in vitro look . [Thesis]. Penn State University; 2013. Available from: https://submit-etda.libraries.psu.edu/catalog/17496

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Penn State University

3. Riddle, Ryan Christopher. Biophysical Regulation of Human Mesenchymal Stem Cell Proliferation .

Degree: 2008, Penn State University

URL: https://submit-etda.libraries.psu.edu/catalog/7707

► Osteoporosis, a disease characterized by low bone mass and increased fracture susceptibility, affects more than 10 million Americans and an additional 34 million are at… (more)

▼ Osteoporosis, a disease characterized by low bone mass and increased fracture susceptibility, affects more than 10 million Americans and an additional 34 million are at risk of developing this disease. As our population continues to age these numbers are likely to grow significantly. Estimates of the economic burden of treating this disease in 2005 are on the order of $17 billion and are expected to increase by as much as 50% by 2025. As a result, the development of new therapeutic techniques designed to enhance bone formation and strength is a necessity. One way to achieve such goals is to harness the proliferation and differentiation potential of mesenchymal stem cells (MSCs) derived from skeletal tissue. MSCs provide a source of new bone-forming osteoblasts important for skeletal homeostasis, but the factors that regulate the proliferation and differentiation of MSCs are not completely understood. Mechanical signals are widely accepted regulators of skeletal homeostasis, such that the addition of exogenous mechanical load enhances osteoblastic bone formation while inhibiting osteoclastic bone resoption. Current hypotheses suggest that the deformation of bone in response to an applied load generate substrate strains that drive the movement of interstitial fluid and bone cells sense this fluid movement in the form of chemotransport or a shear stress across cell bodies and processes. Indeed, numerous in vitro studies suggest that both osteoblastic and osteocytic cells respond to the predicted physiologic levels of fluid shear stress by releasing paracrine factors necessary for the anabolic response of bone to mechanical loads. It is likely that fluid flow also regulates the behavior of MSCs, but there is little experimental evidence for this and the signaling cascades activated in MSCs in response to fluid flow have not been examined. Thus the goals of this thesis are three-fold: 1) to examine the effect of oscillatory fluid flow on human mesenchymal stem cell (hMSC) proliferation and to identify candidate signaling cascades involved in this response; 2) to identify the factor that initiates the activation of these signaling cascades; and, 3) to identify the biophysical signal that hMSCs perceive. One hour of fluid flow exposure induced a significant increase in cellular proliferation over static controls, indicating that like osteoblasts and osteocytes, hMSCs are responsive to fluid flow. Since intracellular calcium is a vital mediator of the processes by which extracellular signals are conveyed to the cell’s interior, we next examined whether calcium signaling pathways contribute to the effect of fluid flow on hMSC proliferation. Fluid flow exposure triggered a robust, but transient increase in intracellular calcium concentration that was partially mediated by the activation of phospholipase C. Increased intracellular calcium concentration stimulated the activation of the protein phosphatase calcineurin and the nuclear translocation of its target transcription factor, nuclear factor of activated T… Advisors/Committee Members: Chair%22%29&pagesize-30">Henry Joseph Donahue, Committee Chair/Co-Chair, Sarah Bronson, Committee Member, Douglas Cavener, Committee Member, Christopher J Lynch, Committee Member, Timothy Ritty, Committee Member.

Subjects/Keywords: Osteoporosis; Mesenchymal stem cell; Orthopaedics

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Riddle, R. C. (2008). Biophysical Regulation of Human Mesenchymal Stem Cell Proliferation . (Thesis). Penn State University. Retrieved from https://submit-etda.libraries.psu.edu/catalog/7707

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Riddle, Ryan Christopher. “Biophysical Regulation of Human Mesenchymal Stem Cell Proliferation .” 2008. Thesis, Penn State University. Accessed March 06, 2021. https://submit-etda.libraries.psu.edu/catalog/7707.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Riddle, Ryan Christopher. “Biophysical Regulation of Human Mesenchymal Stem Cell Proliferation .” 2008. Web. 06 Mar 2021.

Vancouver:

Riddle RC. Biophysical Regulation of Human Mesenchymal Stem Cell Proliferation . [Internet] [Thesis]. Penn State University; 2008. [cited 2021 Mar 06]. Available from: https://submit-etda.libraries.psu.edu/catalog/7707.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Riddle RC. Biophysical Regulation of Human Mesenchymal Stem Cell Proliferation . [Thesis]. Penn State University; 2008. Available from: https://submit-etda.libraries.psu.edu/catalog/7707

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Penn State University

4. Leiby, Melanie Ann. Evaluation of BAC-Based Reporters for the Study of Human Telomerase .

Degree: 2008, Penn State University

URL: https://submit-etda.libraries.psu.edu/catalog/7450

► The ongoing efforts to sequence eukaryotic genomes have revealed that contrary to initial predictions, more complex organisms do not necessarily have more complex genomes or… (more)

▼ The ongoing efforts to sequence eukaryotic genomes have revealed that contrary to initial predictions, more complex organisms do not necessarily have more complex genomes or more genes. Instead, it has been shown that higher eukaryotes have more complex gene regulatory mechanisms, leading to increased organismal complexity. Understanding the ways in which genes are regulated is critical to understanding how organisms function in normal and diseased states. Many techniques and model systems have been used to study gene regulation, including transgenic mice and cell lines and promoter analysis via reporter genes. Some of the biggest problems when studying gene regulation are the susceptibility of transgenes to position effect variegation (PEV) and copy number dependence. To alleviate these problems, techniques have been developed to introduce transgenes in a single copy at predetermined genomic loci. Another concern when using standard transgenes to study gene regulation is that they do not always mimic the expression patterns of the endogenous locus, either because they do not contain all appropriate regulatory elements and/or are unable to re-form the native chromatin environment. The use of yeast, bacterial, and P1 artificial chromosomes (YACs, BACs, and PACs, respectively) as transgenes has been shown to increase the likelihood that a transgene will be expressed in an endogenous manner due to the increased amount of genomic sequence they harbor. Therefore, transgenics created using artificial chromosomes targeted in a single copy to a predetermined genomic locus should be very beneficial to the study of gene regulation. One gene that would benefit from such a system is human telomerase reverse transcriptase (TERT). TERT encodes a reverse transcriptase specific for telomeres, the tandemly repeated sequence located at the ends of all eukaryotic chromosomes that, in addition to their associated proteins, serve as caps to prevent critical genetic information from being lost due to the end replication problem and protect chromosomes from end-to-end fusions. In humans, TERT is expressed at high levels during embryogenesis, but in adult somatic cells, TERT is silenced; however, in 85-90% of all human tumors, telomerase is reactivated. The correlation between a lack of telomerase activity and hTERT mRNA seems to suggest telomerase expression is regulated predominantly at the level of transcription; however, despite almost 25 years of study, the mechanisms of hTERT regulation have remained elusive. One of the main reasons for this is the lack of a powerful model system. Mice, which are often used to study human genes, are not good models for studying hTERT because mTERT expression is much more promiscuous than that of hTERT and their overall telomere length is much longer. Additionally, transiently expressed, hTERT promoter-based reporters do not always mimic the endogenous telomerase activity of the cells into which they are introduced. We hypothesized that an hTERT reporter created from a BAC introduced in… Advisors/Committee Members: Chair%22%29&pagesize-30">Henry Joseph Donahue, Committee Chair/Co-Chair, Sarah Bronson, Committee Member, Kristin Ann Eckert, Committee Member, Mary Judith Tevethia, Committee Member.

Subjects/Keywords: bacterial artificial chromosomes; transcriptional regulation; telomerase; recombineering

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Leiby, M. A. (2008). Evaluation of BAC-Based Reporters for the Study of Human Telomerase . (Thesis). Penn State University. Retrieved from https://submit-etda.libraries.psu.edu/catalog/7450

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Leiby, Melanie Ann. “Evaluation of BAC-Based Reporters for the Study of Human Telomerase .” 2008. Thesis, Penn State University. Accessed March 06, 2021. https://submit-etda.libraries.psu.edu/catalog/7450.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Leiby, Melanie Ann. “Evaluation of BAC-Based Reporters for the Study of Human Telomerase .” 2008. Web. 06 Mar 2021.

Vancouver:

Leiby MA. Evaluation of BAC-Based Reporters for the Study of Human Telomerase . [Internet] [Thesis]. Penn State University; 2008. [cited 2021 Mar 06]. Available from: https://submit-etda.libraries.psu.edu/catalog/7450.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Leiby MA. Evaluation of BAC-Based Reporters for the Study of Human Telomerase . [Thesis]. Penn State University; 2008. Available from: https://submit-etda.libraries.psu.edu/catalog/7450

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Penn State University

5. Genetos, Damian C. ATP Release and Purinergic Mechanotransduction in Bone Cells.

Degree: 2008, Penn State University

URL: https://submit-etda.libraries.psu.edu/catalog/6532

► Osteoporosis is a disease of the skeleton that is characterized by fragile bones, which increases the risk of skeletal fracture. According to the latest report… (more)

▼ Osteoporosis is a disease of the skeleton that is characterized by fragile bones, which increases the risk of skeletal fracture. According to the latest report from the Surgeon General of the United States, 10 million Americans over the age of 50 have osteoporosis, and 34 million are at risk [1]. Osteoporosis causes 1.5 million skeletal fractures per year at an annual cost of $12.2–17.9 billion per year [2]. As the population continues to age [3], this annual expenditure will surely rise as well. Consequently, osteoporosis prevention is at the forefront of orthopaedic research. One method to prevent osteoporosis is to increase the formation of new bone while preventing the resorption of older bone. A wealth of reports have demonstrated that mechanical loads can regulate skeletal architecture by increasing the activity of bone-forming osteoblasts and inhibiting the activity of bone-resorbing osteoclasts. This would strengthen the skeleton and thereby reduce the risk of osteoporosis. What continues to perplex orthopaedic investigators are the cellular mechanisms whereby external mechanical forces are perceived by cells of the osteoblastic lineage and transduced into an anabolic response (i.e., formation of new bone by osteoblasts). Movement of pericellular fluid, or fluid flow, induced by mechanical loads appears to be the most likely localized signal perceived by osteoblasts and osteocytes. The application of fluid flow to these cell lineages induces a rapid, yet transient increase in cytosolic calcium (Ca2+i) that requires both calcium entry into the cell and calcium release from cytoplasmic stores [4]; changes in Ca2+i are implicated in the regulation of a multitude of cellular responses ranging from acute (such as kinase activation [5]) to trophic (i.e., proliferation [6-8]). One signaling molecule that is able to induce both calcium entry and calcium release in osteogenic cells is adenosine triphosphate (ATP) which can activate both ionotropic P2X and metabotropic P2Y receptors [9]. Indeed, the importance of P2 receptors in the calcium response of osteoblasts to fluid flow was recently demonstrated by You et al. [10]. However, the mechanism(s) whereby cytosolic ATP is released from an osteoblast or osteocyte in response to fluid flow has not been described. The overall aims of this thesis were to address how ATP is released from osteoblasts and osteocytes and to further elucidate the importance of P2 receptor activation by ATP in bone cell mechanotransduction. We first examined whether osteoblasts, as the cells directly responsible for the formation of new bone, release ATP in response to fluid flow. Using a steady, laminar flow system with a flow rate that induced a shear rate of 12 dynes/cm2, we found that conditioned media from osteoblasts exposed to fluid flow for 5 minutes contained approximately 10-fold more ATP than did conditioned media from static osteoblasts (59.8+15.7 vs 6.2+1.8 nM). We next used a Harvard pump one-pass system, which perfused fresh media across the osteoblasts, to examine the time… Advisors/Committee Members: Chair%22%29&pagesize-30">Henry Joseph Donahue, Committee Chair/Co-Chair, Randall L Duncan, Committee Member, Blaise Peterson, Committee Member, David A Antonetti, Committee Member, Shao Cong Sun, Committee Member, Neil Sharkey, Committee Member.

Subjects/Keywords: bone; osteoblast; osteocyte; ATP; hemichannel; prostaglandin; mechanical loading; fluid flow

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Genetos, D. C. (2008). ATP Release and Purinergic Mechanotransduction in Bone Cells. (Thesis). Penn State University. Retrieved from https://submit-etda.libraries.psu.edu/catalog/6532

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Genetos, Damian C. “ATP Release and Purinergic Mechanotransduction in Bone Cells.” 2008. Thesis, Penn State University. Accessed March 06, 2021. https://submit-etda.libraries.psu.edu/catalog/6532.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Genetos, Damian C. “ATP Release and Purinergic Mechanotransduction in Bone Cells.” 2008. Web. 06 Mar 2021.

Vancouver:

Genetos DC. ATP Release and Purinergic Mechanotransduction in Bone Cells. [Internet] [Thesis]. Penn State University; 2008. [cited 2021 Mar 06]. Available from: https://submit-etda.libraries.psu.edu/catalog/6532.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Genetos DC. ATP Release and Purinergic Mechanotransduction in Bone Cells. [Thesis]. Penn State University; 2008. Available from: https://submit-etda.libraries.psu.edu/catalog/6532

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

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